Complication of portal

hypertention

Variceal bleeding
Is a common manifestation of chronic liver disease,
however, gastrointestinal bleeding can also occur as the result of peptic ulceration,
which is more common in patients with liver disease than in the general population

Management of Variceal bleeding

The priority in acute bleeding from oesophageal varices is to restore
the circulation with blood and plasma, not least because shock
reduces liver blood flow and causes further deterioration of liver
function.
All patients with cirrhosis and gastrointestinal bleeding should receive
prophylactic broad-spectrum antibiotics, such as oral ciprofloxacin or
intravenous cephalosporin, because sepsis is common and treatment
with antibiotics has been shown to improve outcome.
Emergency management of bleeding

SBP= spontaneous bacterial

peritonitis

The measures used to control acute variceal bleeding include

endoscopic therapy (banding or sclerotherapy),
balloon tamponade and oesophageal transection.
Active bleeding at endoscopy may make endoscopic therapy
difficult; in such cases, bleeding should be controlled by
balloon tamponade prior to endoscopic therapy

1)Banding ligation and 2)Pharmacological reduction

sclerotherapy
It stops variceal bleeding in 80% of
patients and can be repeated if
bleeding recurs.
Banding is repeated every 1-2
weeks until the varices are
obliterated.
Banding is associated with less risk
of oesophageal perforation and
oesophageal strictures
Sclerotherapy now been largely
abandoned in preference to banding
ligation.
Prophylactic acid suppression with
proton pump inhibitors reduces the
risk of secondary bleeding from
banding-induced ulceration.
of portal venous pressure
Is less important than banding in
preventing rebleeding, but is
useful in reducing active bleeding
while endoscopy is being
arranged.
Terlipressin is the current drug
of choice and releases the
vasoconstrictor, vasopressin,
over several hours in amounts
sufficient to reduce the portal
pressure without producing
systemic effects. It is given in a
dose of 2 mg i.v. 6-hourly until
bleeding stops, and then 1 mg 6-
hourly for a further 24 hours
3)Balloon tamponade :-
This technique employs a Sengstaken-Blakemore tube possessing two
balloons which exert pressure in the fundus of the stomach and in the
lower oesophagus respectively Current modifications incorporate
additional lumens to allow material to be aspirated from the stomach and
from the oesophagus above the oesophageal balloon .
Self-expanding removable oesophageal stents are a new alternative to the
Sengstaken tube in patients with bleeding oesophageal, in contrast to gastric,
varices
4)Transjugular intrahepatic portosystemic stent shunting
(TIPSS):-
This technique uses a stent placed between the portal vein and the
hepatic vein within the liver to provide a portosystemic shunt and
therefore reduce portal pressure
The procedure is carried out under radiological control via the internal
jugular vein; prior patency of the portal vein must be determined
angiographically, coagulation deficiencies may require correction with
fresh frozen plasma, and antibiotic cover is provided.
Successful shunt placement stops and prevents variceal bleeding. Further
bleeding necessitates investigation and treatment (e.g. angioplasty)
because it is usually associated with shunt narrowing or occlusion.

Hepatic encephalopathy may occur following TIPSS and is managed by

reducing the shunt diameter. Although TIPSS is associated with less
rebleeding than endoscopic therapy, survival is not improved
5)Portosystemic shunt surgery
portosystemic shunts are now indicated for patients in whom other treatments
have not been successful and are offered only to those with good liver function.
It prevents recurrent bleeding, but carries a high mortality and often leads to
encephalopathy.

I. Non-selective portacaval shunts can divert the majority of the portal

blood away from the liver, rendering patients liable to post-operative liver
failure and hepatic encephalopathy.
II. Selective shunts (such as the distal splenorenal shunt); are
associated with less post-operative encephalopathy, but with the passage
of time liver portal blood flow falls and encephalopathy may supervene.
. Survival is not prolonged, as death from liver failure may occur.

6)Oesophageal transection:-performed with a stapling gun, although this carries some

risk of subsequent oesophageal stenosis and is normally combined with splenectomy.
The operative morbidity and mortality are considerable and the procedure is now rarely
used
 I) Primary prevention of II)Secondary prevention of
variceal bleeding variceal bleeding
Propranolol (80-160 mg/day) or Beta-blockers have also been
nadolol is effective in reducing used as a secondary measure to
portal venous pressure. prevent recurrent variceal
These drugs at doses which bleeding following banding.
reduce the heart rate by 25% has So the secondary prevention
been shown to be effective in the Banding first & then -
primary prevention of variceal Primary prevention of variceal
blockers
bleeding, which is the most bleeding
'In patients with cirrhosis,
important complication of portal
treatment with propranolol
hypertension.
reduces :-
The efficacy of -
1. Variceal bleeding by
adrenoceptor antagonists (- 47%
blockers) in primary 2. Death from bleeding
prevention is similar to that by 45%
of prophylactic banding. 3. Overall mortality by
22%
Prognosis:-
The mortality following a variceal bleed has improved to around
15% overall but still is about 45% in those with poor liver
function, i.e. Child-Pugh C patients .
In the presence of portal hypertension, the risk of a variceal bleed
occurring within 2 years varies from 7% for small varices up to 30% for
large varices.
Acute liver failure
is an uncommon but serious syndrome presented with mental
changes progressing from confusion to stupor and coma, and a
progressive deterioration in liver function.
The syndrome was originally defined further as occurring within 8
weeks of onset of the precipitating illness, in the absence of
evidence of pre-existing liver disease.

whil
e

Hepatic encephalopathy represents a

deterioration in chronic liver disease.
 Acute liver failure can be classified
according to the interval between
onset of jaundice and
encephalopathy into:-
1. Hyperacute.
2. Acute.
3. Subacute.

These reflect differences in presentation and

outcome of acute liver failure
 Classification of acute liver failure

Time: jaundice
to
encephalopath Common
Type y Cerebral oedema causes
Hyperacute < 7 days Common Viral,
paracetamol
Acute 8-28 days Common Cryptogenic,
drugs
Subacute 29 days-12 Uncommon Cryptogenic,
weeks drugs
 Clinical features:-
Cerebral disturbance (hepatic encephalopathy) is the
cardinal manifestation of acute liver failure, but in the early
stages this can be mild and episodic.

Initial clinical features are Cerebral oedema may occur due to

often subtle and include:-
Reduced alertness and
poor concentration
Progressing through
behavioral abnormalities
such as restlessness and
aggressive outbursts, to
drowsiness and coma
increased intracranial pressure
causing :-
1. unequal or abnormally reacting
pupils, fixed pupils,
2. Hypertensive episodes,
bradycardia.
3. Hyperventilation, profuse sweating
4. local or general myoclonus, focal
fits or decerebrate posturing
5. Papilloedema occurs rarely and is a
late sign.

General symptoms include weakness,

nausea and vomiting. Right
hypochondrial discomfort is an occasional
feature.
 Clinical signs

Jaundiced, except in Reye's syndrome when jaundice is rare.

Occasionally, death may occur in fulminant cases of acute liver
failure before jaundice develops.
Fetor hepaticus can be present.
The liver is usually of normal size but later becomes smaller.

Hepatomegaly is unusual and, in the presence of a sudden onset

of ascites, suggests venous outflow obstruction as the cause
(Budd-Chiari syndrome).

Splenomegaly is uncommon and never prominent.

Ascites and oedema are late developments and may be a

consequence of fluid therapy.
Causes of acute liver
failure
 How to grade hepatic encephalopathy clinically

Clinical grade Clinical signs

Grade 1 Poor concentration, slurred speech, slow
mentation, disordered sleep rhythm

Grade 2 Drowsy but easily rousable, occasional

aggressive behaviour, lethargic

Grade 3 grade hepatic encephalopathy

Marked confusion, drowsy, clinically
sleepy but responds
to pain and voice, gross disorientation

Grade 4 Unresponsive to voice, may or may not respond

to painful stimuli, unconscious
Investigations
Investigations to Adverse prognostic
determine the cause of criteria in acute liver
acute liver failure:- failure*
1. Toxicology screen of blood and
urine
2. HBsAg, IgM anti-HBc
1. H+ > 50 nmol/L (pH < 7.3)
3. IgM anti-HAV
at or beyond 24 hours
following the overdose
4. Anti-HEV, HCV,
cytomegalovirus, herpes or
simplex, Epstein-Barr virus 2. Serum creatinine > 300
5. Ceruloplasmin, serum copper, mol/L ( 3.38 mg/dL) plus
urinary copper, slit-lamp eye prothrombin time > 100
examination seconds plus
6. Autoantibodies: ANF, ASMA, encephalopathy grade 3 or
LKM
4
7. Immunoglobulins
8. Ultrasound of liver and Doppler
of hepatic veins
Adverse prognostic criteria in acute liver failure for
Non-paracetamol cases

A. Prothrombin time > 100 seconds

or
B. Any three of the following:
1. Jaundice to encephalopathy time > 7 days
2. Age < 10 or > 40 years
3. Indeterminate or drug-induced causes
4. Bilirubin > 300 mol/L ( 17.6 mg/dL)
5. Prothrombin time > 50 seconds
or
C. Factor V level < 15% and encephalopathy grade 3 or 4
 Investigations

Hepatitis B core IgM antibody is the best screening test for acute hepatitis B
infection, as liver damage is due to the immunological response to the virus
which has often been eliminated and the test for HBsAg may be negative.
The PT rapidly becomes prolonged as coagulation factor synthesis fails; it of
greatest prognostic value and should be carried out at least twice daily. Its
prognostic importance emphasises the necessity of avoiding the use of
fresh frozen plasma to correct raised prothrombin time in acute liver
failure, except in the setting of frank bleeding.
Factor V levels can be used instead of the prothrombin time to assess the
degree of liver impairment.
The plasma bilirubin reflects the degree of jaundice.

Plasma aminotransferase activity is particularly high after paracetamol

overdose, reaching 100-500 times normal, but falls as liver damage progresses
and is not helpful in determining prognosis.

Plasma albumin remains normal unless the course is prolonged.

Percutaneous liver biopsy is contraindicated because of the severe
coagulopathy, but biopsy can be undertaken using the transjugular
route.
 Management
Patient should be treated in a high-dependency or ICU as soon as
progressive prolongation of the PT occurs or hepatic
encephalopathy is identified.
Conservative treatment aims to maintain life in the hope that
hepatic regeneration will occur, but early transfer to a specialised
transplant unit should always be considered.
N-acetylcysteine therapy may improve outcome, particularly in
patients with acute liver failure due to paracetamol poisoning.
Liver transplantation is an increasingly important treatment
option for acute liver failure, and criteria have been developed to
identify patients unlikely to survive without a transplant.
Patients should, wherever possible, be transferred to a transplant
centre before these criteria are met to allow time for assessment
and to maximise the time for a donor liver to become available.
Survival following liver transplantation for acute liver failure is
improving, and 1-year survival rates of about 60% can be
expected.
 Monitoring in acute liver failure
Neurological
Intracranial pressure
monitoring (specialist units)
Conscious level
Cardiorespiratory Pulse
Blood pressure
Central venous pressure
Respiratory rate
Fluid balance
Hourly output (urine,
vomiting, diarrhoea)
Input: oral, intravenous
Blood analyses
Arterial blood gases
Peripheral blood count (including
platelets)
Sodium, potassium, HCO3-,
calcium, magnesium
Creatinine, urea
Glucose (2-hourly in acute phase)
Prothrombin time
Infection surveillance
Cultures: blood, urine, throat,
sputum, cannula sites
Chest X-ray
Temperature
 Complications of acute liver failure

1. Encephalopathy and cerebral oedema

2. Hypoglycaemia
3. Metabolic acidosis
4. Infection (bacterial, fungal)
5. Renal failure
6. Multi-organ failure (hypotension and respiratory failure)
 Hepatic encephalopathy
Is a neuropsychiatric syndrome caused by chronic liver
disease.
Features include changes of intellect, personality, emotions and
consciousness.
The earliest features are very mild and easily overlooked but, as
the condition becomes more severe, apathy, inability to
concentrate, confusion, disorientation, drowsiness, slurring of
speech and eventually coma develop. Convulsions sometimes
occur.
Clinical Signs:-
1. flapping tremor (asterixis).
2. Inability to perform simple mental arithmetic tasks or to
draw objects such as a star (constructional apraxia).
3. Hyper-reflexia and bilateral extensor plantar responses as
the condition progresses.
4. Fetor hepaticus, a sweet musty odour to the breath, is
usually present but is more a sign of liver failure and
portosystemic shunting than of hepatic encephalopathy.
5. Rarely, chronic hepatic encephalopathy (hepatocerebral
degeneration)
Hepatic gives rise
encephalopathy tocauses
rarely variable combinations
focal of
neurological signs, and if
cerebellar dysfunction,
these Parkinsonian
are present, syndromes,
other causes must spastic
be sought
 Pathophysiology
Hepatic encephalopathy is thought to be due to a disturbance of brain
function provoked by circulating neurotoxins that are normally metabolised
by the liver.

Neurotoxins causing the encephalopathy, they are thought to be

mainly nitrogenous substances produced in the gut, at least in part by
bacterial action,
Ammonia has traditionally been considered an important factor and
ammonia-induced alteration in astrocyte glutamine and glutamate
concentrations.
Recent interest has focused on -aminobutyric acid as a mediator,
along with other factors such as octopamine, amino acids,
mercaptans and fatty acids which can act as neurotransmitters.
These substances are normally metabolised by the healthy liver and
therefore excluded from the systemic circulation.
Most affected patients have evidence of liver failure and portosystemic
shunting of blood, but the balance between these varies from
individual to individual.
Some degree of liver failure is a key factor, as portosystemic
shunting of blood alone hardly ever causes encephalopathy
Factors precipitating hepatic encephalopathy
The degree of encephalopathy can be graded from
1 to 4,which will assess grade & assessing response
to therapy.
(Same grading for hepatic failure)
Investigations & Diagnosis:-
The diagnosis can usually be made clinically, but when
doubt exists;
1. Electroencephalogram (EEG) shows diffuse slowing
of the normal alpha waves with eventual
development of delta waves.
2. Arterial ammonia is usually increased in patients
with hepatic encephalopathy. this investigation is of
little or no diagnostic value as increased
concentrations can occur in the absence of clinical
encephalopathy.
 Management of hepatic encephalopathy
Chronic or refractory hepatic encephalopathy is one of the main indications
for liver transplantation.
1. Treat or remove precipitating causes.
2. Dietary protein restriction is rarely needed and is no longer
recommended as first-line treatment because it is unpalatable and can
lead to a worsening nutritional state in already malnourished patients.
3. Lactulose (15-30 mL 8-hourly) is a disaccharide which is taken orally
and reaches the colon intact, to be metabolised by colonic bacteria. The
dose is increased gradually until the bowels are moving twice daily.
It produces an osmotic laxative effect, reduces the pH of the
colonic content, thereby limiting colonic ammonia absorption, and
promotes the incorporation of nitrogen into bacteria. Lactitol is a
rather more palatable alternative to lactulose, with a less explosive action
on bowel function.
4. Neomycin (1-4 g 4-6-hourly) is an antibiotic which acts by
reducing the bacterial content of the bowel. It can be used in addition or as
an alternative to lactulose if diarrhoea becomes troublesome. Neomycin is
poorly absorbed from the bowel but sufficient gains access to the body to
contraindicate its use when uraemia is present. It is less desirable than
lactulose for long-term use; ototoxicity is the main deleterious effect
and so neomycin is now rarely used.
Thanks